Reimann J, Rudolphi A, Claesson M H
Institute of Microbiology, Ulm University, FRG.
Int Immunol. 1991 Jul;3(7):657-63. doi: 10.1093/intimm/3.7.657.
Young severe combined immunodeficiency (scid) mice completely lack immunocompetent lymphocytes. Limiting numbers of purified CD4+ T cells from allotype-congenic BALB/c (Igha) donor mice were transplanted into 3-week-old scid (Ighb) recipient mice. Splenic CD4+ T cells were recovered from transplanted scid mice 10-12 weeks post-transfer and established as T cell lines in culture. These T cell populations proliferated in vitro in response to syngeneic stimulator cells. T cell clones derived in vitro from these T cell lines displayed selfreactive recognition specificity: these CD4+ T cells proliferated in vitro in response to syngeneic/congeneic but not allogeneic stimulator cells. Cloned selfreactive T cells retransplanted into young scid recipients were engrafted into spleens of secondary recipients, did not induce autoimmune disease but stimulated development of scid-derived (Ighb), IgM-producing B cells (B cell leakiness).
幼年重症联合免疫缺陷（scid）小鼠完全缺乏具有免疫活性的淋巴细胞。将来自同种异型同基因BALB/c（Igha）供体小鼠的有限数量的纯化CD4 + T细胞移植到3周龄的scid（Ighb）受体小鼠中。在移植后10 - 12周从移植的scid小鼠中回收脾CD4 + T细胞，并在培养中建立为T细胞系。这些T细胞群体在体外对同基因刺激细胞产生增殖反应。从这些T细胞系体外衍生的T细胞克隆表现出自身反应性识别特异性：这些CD4 + T细胞在体外对同基因/同种基因而非异基因刺激细胞产生增殖反应。克隆的自身反应性T细胞重新移植到幼年scid受体中后，植入二级受体的脾脏中，未诱导自身免疫性疾病，但刺激了scid来源的（Ighb）、产生IgM的B细胞（B细胞渗漏）的发育。
